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Transcription Factors
Post-translational modifications and subcellular localizations modulate transcription factors, generating a code that is deciphered into an activity. We describe our current understanding of these
Plasminogen activator inhibitor-1 is a critical downstream target of p53 in the induction of replicative senescence
TLDR
It is reported that suppression of the p53 target gene encoding plasminogen activator inhibitor-1 (PAI-1) by RNA interference leads to escape from replicative senescence both in primary mouse embryo fibroblasts and primary human BJ fibro Blasts.
Suppression of experimental autoimmune encephalomyelitis by oral administration of myelin basic protein and its fragments
TLDR
It is reported that experimental autoimmune encephalomyelitis can be suppressed in Lewis rats by the oral administration of myelin basic protein (MBP), suggesting that suppressor determinants exist in the MBP molecule distinct from the encephalitogenic region.
TGF-β1 → SMAD/p53/USF2 → PAI-1 transcriptional axis in ureteral obstruction-induced renal fibrosis
TLDR
Mechanisms discussed here appear to be operative in other renal fibrotic disorders and are relevant to the global issue of tissue fibrosis, regardless of organ site.
Reaction of monosaccharides with proteins: possible evolutionary significance.
TLDR
The emergence of glucose as the primary metabolic fuel may be due in part to the high stability of its ring structure which limits potentially deleterious nonenzymatic glycosylation of proteins.
Kinetic analysis of the nonenzymatic glycosylation of hemoglobin.
  • P. Higgins, H. Bunn
  • Chemistry, Medicine
    The Journal of biological chemistry
  • 25 May 1981
TLDR
These experiments provide direct chemical evidence for an aldimine precursor in the nonenzymatic glycosylation of protein in normal and diabetic red cells.
TGF-β signaling in tissue fibrosis: redox controls, target genes and therapeutic opportunities.
TLDR
A novel role for p53 in TGF-β1-induced PAI-1 transcription that involves ROS generation and p53/SMAD interactions is suggested to have therapeutic implications in the management of fibrotic disorders.
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